Childhood socioeconomic status (SES) has been associated with adult cardiovascular disease, but the mechanisms of how this occurs have not been fully explored. Furthermore, low SES is associated with the co-occurrence of multiple social (i.e., increased violence exposure), physical (i.e., higher air pollution levels, poor access to recreational facilities and access to fresh fruits and vegetables) and behavioral (i.e., poor diet, low physical activity, tobacco use) risk factors associated with cardiovascular disease. However, exposures to these factors during childhood and adolescence have not been evaluated with respect to their role in the development of metabolic and cardiovascular risk profiles in a prospective study. Given the complexity of interactions (individual and neighborhood, social and physical) a life course framework may be a fruitful approach to exploring the individual exposures and social attributes of neighborhoods that contribute to the development of metabolic and cardiovascular risk profiles. This proposal aims to examine the contribution of social stressors and physical environment experienced at both the individual and neighborhood level during adolescence, and their interactions on the development of cardiovascular and metabolic risk profiles (i.e., blood pressure, CRP, Hemoglobin A1c, BMI, waist circumference, total cholesterol, triglycerides, LDL, HDL, non-HDL cholesterol). The research goals of this proposal will be achieved with two projects. First, using the National Longitudinal Study of Adolescent Health (Add Health), a longitudinal cohort of adolescents followed through adulthood, I will employ a life course approach to determine whether social stressors (i.e., interpersonal violence, school and community violence) and physical environment (i.e., access to food stores, proximity to parks and recreation) experienced in adolescence plays a role in the development of metabolic and cardiovascular risk profiles in adulthood. Interactive effects between social and physical environmental factors will also be examined. Second, I will develop a primary collection cross-sectional study of 100 adolescents to examine the mediating effect of diet (not available in Add Health) and the modifying effects of air pollutants (also not available in the Add Health study) on the stress-cardiovascular health relationship. I will dedicate no less than 75 percent of my time to a highly structured and intensely focused research experience over the next 5 years, which will extend my expertise in characterizing social and environmental determinants as stressors in relation to physiological outcomes in children and young adults. A career development plan is outlined to gain practical skills in research design and implementation, expertise in statistical models to predict air pollutant levels and structural equation models as well as knowledge in the mechanisms of cardiovascular and metabolic disorders. The career development plan includes: 1) formal graduate course work in survey design, latent statistical models, mechanisms of cardiovascular disease, 2) tutorial with project advisor to learn clinical aspects of cardiovascular and metabolic disorders in adolescents 3) tutorial with advisor to discuss air pollutant modeling strategies 4) interactions with mentoring team to discuss research and career goals and project progress. I will work closely with the mentoring team which collectively has extensive experience in mentoring new clinical investigators, disparities in psychosocial factors, life experiences and cardiovascular disease outcomes, effects of neighborhood environment and cardiovascular disease, and disparities in physical environmental factors. The proposed training, consisting of interactions with mentors and advisors, tutorials and coursework, complements my previous training and experience in social and environmental epidemiologic research and will allow me to develop the necessary transdisciplinary expertise to achieve my goal and successfully transition to independent investigator at the end of this award. The proposed project will focus on a major health problem in the U.S. - cardiovascular disease, particularly its onset during the adolescent years and explore new models of how individual and community factors, in this case exposure to violence and environmental toxins, impact health outcomes. Findings from these studies can inform clinical practice in chronic disease prevention so that providers and policymakers alike can tailor age appropriate interventions to adolescents and young adults that jointly address the individual as well as the environmental context to more effectively reduce cardiovascular disease risk. PUBLIC HEALTH RELEVANCE: Childhood socioeconomic status (SES) has been associated with adult cardiovascular disease, but the mechanisms of how this occurs have not been fully explored. Furthermore, low SES is associated with the co-occurrence of multiple social (i.e., increased violence exposure), environmental (i.e., higher air pollution exposure, poor access to recreational facilities or food stores) and behavioral (i.e., poor diet, low physical activity, tobacco use) risk factors associated with cardiovascular disease. However, exposures to these factors during childhood and adolescence have not been evaluated with respect to their role in the development of metabolic and cardiovascular risk profiles in a prospective study. Given the complexity of interactions (individual and neighborhood, social and physical) a life course framework may be a fruitful approach to exploring the individual exposures and social attributes of neighborhoods that contribute to the development of metabolic and cardiovascular risk profiles. This proposal aims to examine the contribution of social stressors and physical environment experienced at both the individual and neighborhood level during adolescence, and their interactions on the development of cardiovascular and metabolic risk profiles (i.e., blood pressure, CRP, Hemoglobin A1c, BMI, waist circumference, total cholesterol, triglycerides, LDL, HDL, non-HDL cholesterol). (End of Abstract)